Research Papers:

MiR-125a suppresses tumor growth, invasion and metastasis in cervical cancer by targeting STAT3

Zhongyi Fan, Hanzhi Cui, Xiaojie Xu, Zhi Lin, Xuelin Zhang, Lei Kang, Baiyu Han, Jing Meng, Zhifeng Yan, Xiang Yan and Shunchang Jiao _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2015; 6:25266-25280. https://doi.org/10.18632/oncotarget.4457

Metrics: PDF 2491 views  |   HTML 3490 views  |   ?  


Zhongyi Fan1,*, Hanzhi Cui2,*, Xiaojie Xu3,*, Zhi Lin1, Xuelin Zhang1, Lei Kang4, Baiyu Han5, Jing Meng1, Zhifeng Yan1, Xiang Yan1, Shunchang Jiao1

1Department of Oncology, PLA General Hospital, Beijing, China

2Department of Oncology, 309th Hospital of PLA, Beijing, China

3Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China

4Department of Nuclear Medicine, Peking University First Hospital, Beijing, China

5Department of Endocrinology and Metablism, 264th Hospital of PLA, Shanxi, China

*These authors have contributed equally to this work

Correspondence to:

Shunchang Jiao, e-mail: [email protected]

Keywords: miR-125a, cervical cancer, cell growth, metastasis, STAT3

Received: March 23, 2015     Accepted: June 30, 2015     Published: July 13, 2015


MiR-125a has been characterized as a tumor suppressor in several cancers. However, the role of miR-125a in cervical cancer is unknown. In this study, we found the expression of miR-125a was downregulated in cervical cancer patients, and negatively correlated with the tumor size, FIGO stage, and preoperative metastasis. Kaplan-Meier analysis showed that miR-125a expression predicted favorable outcome for cervical cancer patients. Dual luciferase assays identified the STAT3 gene as a novel direct target of miR-125a. Functional studies showed that miR-125a overexpression significantly suppressed the growth, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer cells both in vitro and in vivo via decreasing STAT3 expression. Moreover, miR-125a conferred to G2/M cell cycle arrest, accompanied by inhibition of several G2/M checkpoint proteins. Mechanistically, inactivation of miR-125a during cervical carcinogenesis was caused by HPV suppression of p53 expression. Clinically, STAT3, the expression of which, predicted poorer outcome, was inversely correlated with miR-125a in cervical cancer. These data highlight the importance of miR-125a in the cell proliferation and progression of cervical cancer, and indicate that miR-125a may be a useful therapeutic target for cervical cancer.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 4457